32 DOI 10.21608/bmfj.2019.14473.1008

Original article

Clinical and Radiological Predictors For Early Detection

Of Cerebral Vasospasm After Subarachnoid Haemorrhage Abd Elnaser A. Morad

a, Magdy K. Massoud

b, Maged K. F. Botros

a,

. Shaimaa M. kasem

a, Tariq M.Soliman

c .

Background Cerebral vasospasm after subarachnoid haemorrhage is a potentially preventable and

reversible condition where an early identification can prevent or limit cerebral

infarction. Vasospasm may be assessed on a clinical, radiographic, or angiographic

basis.

Aim: Early detection of cerebral vasospasm in a sample of Egyptian patients

presented with spontaneous subarachnoid haemorrhage.

Methods and subjects: In this study we enrolled 40 aSAH patients diagnosed by non-

contrast brain CT and CT angiography and managed by interventional aneurysmal

embolization . Early detection of vasospasm and DCI was assessed on clinical and

radiological basis using transcranial duplex studies (TCD) on the 1st, 3

rd, 5

th, 7

th and

10th

days of the onset of the symptoms . Results: Fourty patients with aSAH , of

them 67.5% developed vasospasm but only 33.3% progressed to DCI. The most

significant day of vasospasm development as detected by TCD was on the 7th

day.The

most common arteries undergoing vasospasm were the MCA followed by the ACA

and lastly the PCA. Clinical scalas on admission as (GCS,HHS,WFNS and Ogilvy

and Carter scale) are highly significant predictors of cerebral vasospasm

Conclusion: Clinical risk factors and the use of TCD are tools for early detection of

vasospasm following SAH. This allows for early therapeutic intervention before

irreversible ischemic neurological deficits take place.

Keywords: Aneurysmal subarachnoid hemorrhage, Transcranial duplex, CT

angiography, Interventional embolization.

Key Messages: Clinical predictors and early detection of cerebral vasospasm by TCD

after spontaneous aneurysmal subarachnoid haemorrhage are highly valuable for

preventing patients from delayed cerebral ischemia occurrence and lessen its impact

irreversible neurological deficits by early therapeutic and endovascular interventions.

Abbreviations:

A.com: Anterior communicating artery; ACA: Anterior cerebral artery; aSAH: Aneurysmal

subarachnoid hemorrhage; AUC: area under curve; CV: Cerebral vasospasm; DBP: Diastolic blood

pressure; DCI: Delayed cerebral ischemia; GCS: Glasgow Coma Scale; HHS: Hunt and Hess Scale;

ICA: Internal carotid artery; MAP: Mean arterial pressure; MCA: Middle cerebral artery; MFV: Mean

flow velocity; NIHSS: National Institute of Health Stroke Scale; P.com: Posterior communicating

artery; PCA: Posterior cerebral artery; RBS: Random blood sugar; ROC curve: Receiver operating

characteristic curve; SAH: Subarachnoid haemorrhage.

a Departement of

Neurology Faculty of

Medicine, Benha

University, MD., Egypt,b

Department of Neurology

and head of

neuropsychiatric

department at El Mataria

teaching hospital, c

Neuropsychiatry at El

Mataria teaching hospital

Corresponding author:

Tariq Mahmoud

Soliman. Address: 110

Reyad street with Gamal

Abdelnaser

street,Tanta,E.Mail: dr.tariqsamy.14@gmail.c

om

Mobile:

00201006711476

Received: 6 July 2019

Accepted: 23 August 2019

Benha Medical Journal

2019, vol 36, issue 2

33 DOI 10.21608/bmfj.2019.14473.1008

Introduction

Cerebral vasospasm is the delayed narrowing of

large capacitance intracranial arteries following

SAH, often associated with radiographic or clinical

evidence of diminished perfusion in the distal

territory of the affected arteries[1][2] and is a

leading contributor to the morbidity and mortality

associated with aSAH [3]It is prolonged sometimes

severe but ultimately reversible

.Symptomatic vasospasm occurs in 20%–30% of

patients with SAH [4]. It usually does not begin

before day 3. Its occurrence peaks during days 7–8

and resolves spontaneously after 21 days [5].

Cerebral vasospasm constitutes a unique

clinicopathological entity characterized by

reversible vasculopathy, impaired auto regulatory

function,[6] Clinical features of cerebral ischemia

after SAH mostly consist of focal neurological

signs, such as aphasia or hemi paresis, or a decrease

in the level of consciousness, typically with gradual

and often fluctuating onset. Signs of cerebral

ischemia are sometimes reversible but may also

progress to cerebral infarction, which can cause

severe disability.[7] Although these clinical deficits

often occur in conjunction with angiographic

evidence of vessel narrowing, each may occur

independently of the other.[8] Transcranial Doppler

(TCD) is a non-invasive ultrasound (US) study

which can detect the blood flow velocities in the

cerebral blood vessels that can be a useful tool in

early prediction of vasospasm after aSAH [9].

Rational thinking suggests that the complications

secondary to vasospasm can be mitigated by

identifying this subgroup of patients early and

instituting appropriate treatment

Aim of the work:

This study aims to predict the occurrence of

cerebral vasospasm using TCD monitoring as a tool

in early diagnosis of cerebral vasospasm following

aSAH.

Patients and Methods

A prospective study was done during a period

of one year starting from April 2017 data was

collected from 40 aSAH patients who were

admitted to the neurovascular unit and ICU of the

neurology department, Mataria Teaching Hospital,

Cairo. The study procedures are approved by ethical

committee Mataria teaching hospital.

Out of the 40 patients only 27 patients

developed cerebral vasospasm. These 27 patients

who developed vasospasm were divided into two

groups: 18 patients who were diagnosed as cerebral

vasospasm without clinical evidence of DCI and 8

patients who were diagnosed as cerebral vasospasm

with clinical evidence of DCI.

Patients excluded from this study were non-

aneurysmal SAH, patients with previous history of

disabling brain injuries causing focal neurological

signs, GCS < 6, patient with decompensate systemic

illness eg. Hepatic, renal and cardiac as all these

will cause deterioration in consciousness level and

any obstacle facing TCD assessment as a closed

temporal window.

Benha Medical Journal, Vol. 36, No. 2, 2019

34

All participants or their first-degree relatives

received detailed information concerning this

research work and its aim and who agreed to

participate signed an informed consent before being

enrolled into the study.

On admission full history taking including

clinical risk factors were assessed (as, blood sugar

and blood pressure on admission) and neurological

examination was done.

All patients were diagnosed by non-contrast

brain CT scan on admission, early four –vessel CT

angiography to localize the site, size and number of

the aneurysms then early interventional

embolization of the aneurysms was then done either

by simple or balloon assisted coiling.

Table (1)

The rate of development of vasospasm regarding risk factors, clinical scales and aneurysmal site, and size

Total

(n = 40)

No vasospasm (n = 13) Vasospasm (n = 27) P value

Age

< 60

27

n (% of total)

10(37%)

n (% of total)

17(63%)

0.484

> 60 13 3(23%) 10(77%)

Sex Males 16 5 (31.25%) 11 (68.75%) 1.000

Females 24 8 (33%) 16 (67%)

Hypertension Non-hypertensive 21 12 (57.1%) 9 (42.9%) 0.006*

Hypertensive 19 1 (5.3%) 18 (94.7%)

Diabetes Non diabetics 34 13 (38.2%) 21 (61.8%) 0.152

Diabetics 6 0 (0%) 6 (100%)

Smoking Non-smokers 29 13 (44.8%) 16 (55.2) 0.007*

Smokers 11 0 (0%) 11 (100%)

Systolic BP <160 (mmHg) 18 7 (38.9%) 11 (61.1%) 0.509

>160 (mmHg) 22 6 (27.2%) 16 (72.8%)

Diastolic BP <100 (mmHg) 19 11 (57.9%) 8 (42.1%) 0.002*

>100 (mmHg) 21 2 (9.5%) 19 (90.5%)

MAP <100 (mmHg) 5 5 (100%) 0 (0%) 0.001*

>100 (mmHg) 35 8 (22.8%) 27 (77.2%)

RBS < 200 (mg/dl) 28 13 (46.4%) 15 (53.6%) 0.001*

> 200 (mg/dl) 12 0 (0%) 12 (100%)

Cholesterol <200 (mg/dl) 38 13 (34.2%) 25 (65.8%) 1.000

>200 (mg/dl) 2 0 (0%) 2 (100%)

GCS <15 19 1 (5.3%) 18 (94.7%) 0.006*

15 21 12 (57.1%) 9 (42.9%)

HHS <3 25 13 (52%) 12 (48%) 0.005*

>3 15 0 (0%) 15 (100%)

Fisher scale <3 19 9 (47.4%) 10 (52.6%) 0.092

>3 21 4 (19%) 17 (81%)

WFNS scale <3 33 13 (39.4%) 20 (59.6%) 0.074

>3 7 0 (0%) 7 (100%)

Aneurysm site MCA 13 0 (0%) 13 (100%) 0.004*

A.com 12 5 (41.7%) 7 (58.3%)

P.com 8 3 (37.5%) 5 (62.5%)

ICA 5 3 (60%) 2 (40%)

PCA 2 2 (100%) 0 (0%)

Aneurysm

size

<11mm 28 12 (42.9%) 16 (57.1%) 0.063

>11mm 12 1 (8.3%) 11 (91.7%)

*significant

Early detection of cerebral vasospasm. Morad et al

35

Using many grading scales on both admission

and assessment of vasospasm severity SAH was

graded clinically by Glasgow Coma Scale (GCS),

Hunt and Hess Scale (HHS) and World Federation

of Neurosurgical Societies (WFNS) scale, and

radiologically by Fisher and Ogilvy and Carter

scales. Daily clinical neurological examination was

done using the NIHSS for early detection of new

focal neurological signs of DCI. The diagnosis of

cerebral vasospasm is based on clinical signs of

progressive impairment in mental status and level of

consciousness or the appearance of new focal

neurologic deficits after the initial SAH that cannot

not attributed to any other structural or metabolic

cause.

TCD studies were done on the 1st, 3

rd, 5

th, 7

th

and 10th

days of the onset of the symptoms to detect

the vasospasm using phased array transducer of

multi-frequency 1–3 MHz, trans-axial

mesencephalic view through the temporal

window. Mean flow velocities (MFV) of middle,

anterior, and posterior cerebral arteries (MCA,

ACA, and PCA respectively) were measured.

Vasospasm is considered when the MFV of the

MCA, ACA, or PCA rises above 120, 90, or 60

cm/s respectively.

The collected data were organized, tabulated

and statistically analyzed using Statistical Package

for Social Studies (SPSS) version 19 created by

IBM, Illinois, Chicago, USA. According to

numerical values the range mean and standard

deviations were calculated. Also, for categorical

variable the number and percentage were calculated

and differences between subcategories were tested

by Fisher or Monte Carlo exact test. The level of

significant was adopted at p<0.05.

Results:

The study included 40 aSAH patients who

fullfilled the inclusion and exclusion criteria with

mean age 51.7 + 11.8 years, females represented

(60%) while males represented (40%)But there was

no significant difference regarding sex between the

different patient groups Considering risk factors for

SAH from history 19 were hypertensive (47.5%), 6

diabetic (15%), and 12 smokers (28%), while

clinical risk variables on admission was as the

following 35 patients with MAP above 100 (87.5%)

,SBP≥ 160mmHg were55% ,DBP≥100mmHg

were52.5% and those with RBS >200 were 30.

While grading on admission was 19 with GCS

<15 (47.5%), 15 with HHS >3 (37.5%), 21 with

Fisher scale >3 (52.5%) and 7 with WFNS scale>3

(17.5%).

Angiography revealed that the ruptured

aneurysmal sites were in the MCA (32.5%), anterior

communicating artery ( A.com) (30%),posterior

communicating artery (P.com) (20%), internal

carotid artery (12.5%) and posterior cerebral artery

Benha Medical Journal, Vol. 36, No. 2, 2019

36

(5%).Regarding the size and number of aneurysms,

12 with aneurysm size >11 mm (30%) and all

patients had single aneurysms.

Those 27aSAH patients who developed TCD

signs of vasospasm; were classified as 11 MCA, 6

ACA, 3PCA and 7 patients with vasospasm in two

arteries at the same time.

Regarding the relation between development

of cerebral vasospasm and demographic and clinical

risk factors 17 with age <60 years (63%), 16

females (59.3%), 18 hypertensive (66.7%), 6

diabetics (22.2%), 11 smokers (40.7%), 16 with

SBP >160(59.2%), 19 with DBP >100 (70.4%), all

patients with MAP >100 (100%), 12 with RBS

>200 (44.4%), 18 with GCS <15 (66.7%), 15 with

HHS >3 (55.5%), 7 with WFNS scale>3 (26%), 13

with MCA aneurysms (48.1%), 7 with A.com

aneurysms (26%) and 11 with aneurysm size >11

mm (40.7%). significant difference between both

patient groups was concluded with hypertension and

smoking as co morbidities and with MAP>100

and RBS >200 as risk factors for vasospasm

The most significant TCD changes related to

cerebral vasospasm was on the 7th

day of the onset

of the symptoms 55.6% but only 33.3% developed

DCI and on the 5th

day was29.2%.

All patients received triple H-therapy and

nimodipine. Iinterventional emobilization of the

aneurysms was done to all patients either by simple

or balloon assisted coiling.

Table (2)

Occurrence of vasospasm and DCI in relation to the day

of TCD measurement

Days

Patients with vasospasm= 27

p with

vasospasm

and

w/o DCI

with vasospasm

andDCI

n % n %

Day 0

0

0.0

0

0.0

1.000

Day 3

Day 5

Day7

Day 10

1

4

1

0

3

100.0

50,0

66.7

100.0

0

4

5

0

0.0

50.0

33.3

0.0

Table (4)

Agreement (sensitivity, specificity) for GCS, WFNS,

HHS, Fisher score, and Ogilvy scale with transcranial

Doppler for detection of vasospasm.

Cut

off

AU

C

P

Sen

siti

vit

y

Spec

ific

ity

GCS < 15 0.808 0.002* 66.7 92.3

WFNS > 3 0.805 0.002* 26.0 100.0

HHS > 3 0.808 0.002* 55.6 100.0

Fisherscore > 3 0.654 0.119 37.0 19.3

Ogilvy scale > 3 0.694 0.050* 22.2 100.0

Table (3)

Occurrence of vasospasm and DCI in relation to MFV of MCA, ACA and PCA measured by

TCD

MFV of

Patients

Without

Patients with vasospasm

Early detection of cerebral vasospasm. Morad et al

37

MCA (cm/s)

vasospasm with vasospasm

w/o DCI

with vasospasm and DCI p

n % n % N %

<120=22

120-149=13

>150=5

22

100.0

0

0.0

0

0.0

0.001*

0

0

0.0

0.0

11

0

84.6

0.0

2

5

15.4

100.0

MFV of

ACA (cm/s)

Patients

Without

Patients with vasospasm

p vasospasm with vasospasm

w/o DCI

with vasospasm and

DCI

n % n % N %

<90=30

90-110=6

>110=4

30

100.0

0

0.0

0

0.0

0.001*

0

0

0.0

0.0

5

0

83.3

0.0

1

4

16.7

100.0

MFV of

PCA (cm/s)

Patients

Without

Patients with vasospasm

p vasospasm with vasospasm

w/o DCI

with vasospasm and

DCI

n % n % n %

<60=35

>60=5

35

100.0

0

0.0

0

0.0

0.001*

0 0.0 0 0.0 5 100.0

*significant

38 DOI 10.21608/bmfj.2019.14473.1008

Discussion:

Symptomatic vasospasm is the clinical

syndrome of delayed cerebral ischemia which

remains the single most important cause of

morbidity and mortality in those patients who

survive the initial bleed. Cerebral vasospasm is

associated with a deterioration in clinical status in

30% of patients after SAH[10].

Regarding risk factors this study revealed that

there was a negative relation between age of

patients and development of CV and DCI. This

observation is in agreement with the work of Kale

and colleagues 11].while Elderly patients may be at

less risk for developing vasospasm, but they do not

tolerate ischemia as well as younger ones do and

therefore develop cerebral infarction more

frequently.[10]

It was found that hypertension and smoking

were most prominent risk factors of vasospasm.This

result was in accordance with de Rooij and

colleagues [12] who considered hypertension and

smoking as a potential predictor of vasospasm. As

other studies reported that the effect of hypertension

on regional cerebral blood flow intracranial

pressure and brain tissue oxygenation after SAH

causing cerebral vasospasm [13].The study declared

that vasospasm following aSAH is more common

among patients with lower GCS, higher HHS scale

and Fisher scale. These observations are in

accordance with Chhor and colleagues [14],

Inagawa and colleagues [15] and Frontera and

colleagues [16] respectively. The study showed that

cerebral vasospasm is common in patients with high

SBP, DBP and MAP on admission. This

observation is in agreement with Nakae and

colleagues [17] who revealed a positive association

between vasospasm and high blood pressure.

It was found that MCA and A.com aneurysms

are the most common aneurysmal sites that develop

cerebral vasospasm which is was in accordance

with Ablaand colleagues [18]. Large size

aneurysms were found to be a risk factor for

cerebral vasospasm. This observation was in

agreement with Macdonald and colleagues [19].The

study showed that mild cases of vasospasm

regressed spontaneously without progression to

DCI while patients with severe vasospasm were

more likely to develop DCI. These data was

evidenced by TCD abnormalities. These results are

in accordance with the work of Aldakkan and

colleagues [20] and with that of Mortimer and

colleagues [21] who specified that severe

angiographic vasospasm is associated with

increased risk of DCI and poorer functional out-

come following aSAH. The 7th

day after aSAH is

the most significant day to develop cerebral

Early detection of cerebral vasospasm. Morad et al

39

vasospasm. This result is in accordance with Sen

and colleagues [22] who stated that vasospasm is

seen in 30% to 70% of angiograms at day 7 after

SAH with and without clinical deficit.This study

showed that TCD is an early detector of vasospasm

and predictor of DCI progression TCD is useful not

only in the early vasospasm diagnosis but also in

the identification of progression and severity

of vasospasm. Therefore, TCD could allow both

early planning of therapeutic interventions as well

as monitoring the effect of these interventions.

Which can save golden hours and allow for early

interventional spasmolytic injection to relieve the

vasospasm. Mortimer and colleagues [21] as well as

Jabbarli and colleagues [23] agreed with and

declared these results.

Conclusion

clinical risk factors ,clinical grading scales with

CD are strong and valuable predictors for early

detection of vasospasm following SAH that save

precious time and allow for early therapeutic and

endovascular interventions.

Acknowledgements: We would like to thank the

Neurology Department, Neuro-sonology,

Neurology ICU, Neuro-intervention teams, Mataria

Teaching Hospital for their great help in patients’

selection, and humbling obstacles during the study.

Authors’ contributions: AEM: participated in

study idea and design, patients’ inclusion, and

manuscript revision. MKM: participated in study

idea and design, patients’ inclusion, collection and

follow up, and manuscript revision. MKF:

participated in the study design, patients’ collection

and manuscript revision. SMK: participated in the

study design, patients’ collection and inclusion and

follow up, statistical analysis, collection of the raw

data, manuscript writing and references collection.

TMS: participated in clinical evaluation of the

patients, collection of the raw data, statistical

analysis, transcranial duplex follows up, manuscript

writing and references collection. All authors read

and approved the final manuscript.

References: 1- Raffaella Pizzolato, Javier M. Romero: TCD in the

diagnosis of subarachnoid hemorrhage vasospasm

in Handbook of Clinical Neurology (2016)

2-Rigamonti Ackery A,Baker AJ.: Transcranial Doppler

monitoring in subarachnoid hemorrhage: a critical tool in

critical care. Can J Anaesth; 55:112-23 (2008)

3. Travis R. Ladner, Scott L. Zuckerman, and J Mocco,

“Genetics of Cerebral Vasospasm,” Neurology Research

International, vol. 2013, Article ID 291895,

Benha Medical Journal, Vol. 36, No. 2, 2019

40

4- Jared A. Greenberg, Thomas P. Bleck, Neuroemergencies

in Critical Care Patients in Handbook of Neuroemergency

Clinical Trials (Second Edition), 2018

5-Ronald J. Sattenberg, David S. Liebeskind, in Stroke (Fifth

Edition), 2011

6-Girish Menon : Vasospasm following aneurysmal

subarachnoid hemorrhage: The search for the elusive wonder-

drug Neurology India (2018)Vol.66 423-425

7-Geraghty, J.R. &Testai, F.D.: Delayed Cerebral Ischemia

after Subarachnoid Hemorrhage: Beyond Vasospasm and

Towards a Multifactorial Pathophysiology. Current

Atherosclerosis Reports (2017) 19: 50

8- Mervyn D.I. Vergouwen Marinus Vermeulen, Jan van Gijn,

Gabriel J.E. Rinkel, Eelco F. Wijdicks, J. Paul Muizelaar, et

al.: Definition of Delayed Cerebral Ischemia After

Aneurysmal Subarachnoid Hemorrhage as an Outcome Event

in Clinical Trials and Observational Studies Stroke. 2010;

41:2391–2395

9. D'Andrea A, Conte M, Scarafile R, Riegler L, Cocchia

R, Pezzullo E et al. Transcranial Doppler Ultrasound: Physical

Principles and Principal Applications in Neurocritical Care

Unit. J CardiovascEchogr. 2016; 26(2):28-41.

10- Philippa Newfield, Intracranial Aneurysms: Vasospasm

and Other Issues in Complications in Anesthesia (Second

Edition), 2007

11-Kale SP, Edgell RC, Alshekhlee A, Haghighi AB, Sweeny

J, Felton J, et al. Age-associated vasospasm in aneurysmal

subarachnoid haemorrhage. J Stroke Cerebrovasc; Dis, 2013;

22: 22-7.

12. De Rooij, Rinkel J.E, Dankbaar, Frijns J.M. Delayed

Cerebral Ischemia after Subarachnoid Hemorrhage: A

Systematic Review of Clinical, Laboratory, and Radiological

Predictors Stroke, 2013; 44: 43-54.

1 13. Meunech E, Horn P, Thome C, Roth H, Philipps M,

Hermann P et al. Effects of hypervolemia and

hypertension on cerebral blood flow, intracranial pressure

and brain tissue oxygenation after subarachnoid

hemorrhage. Crit Care Med 2007; 35:1844–1851.

14. Chor V, Le Manach Y, Clarençon F, Chhor, V., Le

Manach, Y., Clarençon, F., Nouet, A., Daban, J. L.,

Abdennour L, et al. Admission risk factors for cerebral

vasospasm in ruptured brain arteriovenous malformations: an

observational study. Crit Care. 2011; 15(4):R190.

15- Inagawa T, Yahara K, Ohbayashi N. Risk factors

associated with cerebral vasospasm following aneurysmal

subarachnoid hemorrhage. Neurol Med Chir (Tokyo).2014 Jun

17. 54 (6):465-73.

16. Frontera JA, Claassen J, Schmidt JM, Wartenberg KE,

Temes R, Connolly ES Jr, et al. Prediction of symptomatic

vasospasm after subarachnoid hemorrhage: the modified fisher

scale. Neurosurgery. 2006 Jul. 59 (1):21-7

17. Nakae, Ryuta, Hiroyuki Yokota, Daizo Yoshida, Akira

Teramoto. Transcranial Doppler Ultrasonography for

Diagnosis of Cerebral Vasospasm after Aneurysmal

Subarachnoid Hemorrhage: Mean Blood Flow Velocity Ratio

of the Ipsilateral and Contralateral Middle Cerebral Arteries.

Neurosurgery, 2011; 69 (4): 876–83.

18. Abla A, Wilson D, Williamson R, Nakaji P, McDougall C,

Zabramski J, et al.The relationship between ruptured

aneurysm location, subarachnoid hemorrhage clot thickness,

and incidence of radiographic or symptomatic vasospasm in

patients enrolled in a prospective randomized controlled trial.

J Neurosurg 2014; 120: 391–7.

19. Macdonald RL, Rosengart A, Huo D, Karrison T. Factors

associated with the development of vasospasm after planned

surgical treatment of aneurysmal subarachnoid hemorrhage. J

Neurosurg 2003; 99: 644–52.

20. Aldakkan A, Mansouri A, Blessing NR, Alotaibi NM,

Macdonald RL. Predictors of delayed cerebral ischemia in

patients with aneurysmal subarachnoid hemorrhage with

asymptomatic angiographic vasospasm on admission.World

Neurosurg. 2017;97:199–204.

Early detection of cerebral vasospasm. Morad et al

41

21. Mortimer AM, Steinfort B, Faulder K, Bradford C, Finfer

S, Assaad N, et al. The detrimental clinical impact of severe

angiographic vasospasm may be diminished by maximal

medical therapy an intensive endovascular treatment. J

Neurointerv Surg. 2015;7:881–7.

22. Sen J, Afinowi R, Kitchen N and Belli A. intracranial

hemorrhage: aneurysmal, idiopathic, and hypertensive,

chapter 43. 2007; Pages 587-594.

23. Jabbarli R, Gläsker S, Weber J, Taschner C, Olschewski

M, Velthoven VV. Predictors of severity of cerebral

vasospasm caused by aneurysmal subarachnoid hemorrhage. J

Stroke Cerebrovasc Dis. 2013;22(8):1332–9.

To cite this article: Abd Elnaser A. Morad, Magdy K. Massoud, Maged K. F. Botros, . Shaimaa M.

kasem, Tariq M.Soliman. Clinical and Radiological Predictors For Early Detection Of Cerebral Vasospasm After

Subarachnoid Haemorrhage BMFJ, 2019, 36 (2) DOI 10.21608/bmfj.2019.14473.1008 .